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Hypertension. 1998;31:1261-1265

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(Hypertension. 1998;31:1261-1265.)
© 1998 American Heart Association, Inc.


Scientific Contributions

Dietary Sodium Restriction Impairs Endothelial Effect of Insulin

Carmine Vecchione; Carmine Morisco; Luigi Fratta; Luigi Argenziano; Bruno Trimarco; ; Giuseppe Lembo

From the IRCCS "INM NEUROMED," Pozzilli (IS) (C.V., C.M., B.T., G.L.), and the Department of Internal Medicine, School of Medicine, "Federico II" University, Naples (C.V., L.F., L.A., B.T.), Italy.

Correspondence to Giuseppe Lembo, MD, PhD, IRCCS "INM NEUROMED" Località Camerelle, 86077 Pozzilli (IS), Italy. E-mail glembo{at}connect.it

Abstract—Hyperinsulinemia and high salt intake represent two independent cardiovascular risk factors. However, it is still unknown whether the change in dietary salt intake may affect the ability of insulin to stimulate whole-body glucose uptake and to modulate endothelial function. Regarding this latter issue, we have recently demonstrated that insulin enhances endothelial-mediated {alpha}2-adrenergic vasorelaxation. In overnight-fasted, freely moving Wistar-Kyoto rats (10 to 12 weeks old), we assessed whole-body glucose uptake (in milligrams per kilogram per minute) during a euglycemic-hyperinsulinemic clamp (insulin infusion rate, 3 mU · kg-1 · min-1) after 3 weeks of normal (NSD, 2% NaCl), high (HSD, 6% NaCl), and low (LSD, 0.6% NaCl) sodium diet. Three days after the clamp study, rats were killed to assess {alpha}2-adrenergic vasorelaxation evoked by UK 14,304 (10-9 to 10-6 mol/L) in aortic rings in control conditions and after insulin exposure (100 µU/mL). Different sodium intakes did not modify the mean blood pressure or the insulin-stimulated whole-body glucose uptake (NSD: 14±1.2, n=16; HSD: 15.4±1.7, n=14; LSD: 14.8±0.8, n=14; NS). In contrast, we confirmed the ability of insulin to enhance {alpha}2-adrenergic vasorelaxation during NSD and HSD ({Delta}% of maximal relaxation, NSD: from 32±3% to 58±3.4%, n=9, P<0.01; HSD: from 33±3.8% to 59±3.5%, n=8, P<0.01), but this effect was impaired during LSD ({Delta}% maximal relaxation, from 36±1.5% to 36±3.4%, n=8, NS). In conclusion, our data demonstrate that in Wistar-Kyoto rats, changes in dietary salt intake do not modify the insulin-stimulated whole-body glucose uptake. In contrast, LSD impairs the insulin potentiation of {alpha}2-adrenergic vasorelaxation, thus suggesting that dietary salt restriction provokes an impairment of insulin effect on endothelial function.


Key Words: sodium chloride • vasorelaxation • glucose uptake • blood pressure • aortic rings • glucose clamp technique